Hemichorea‐Hemiballism in a Patient with Temporal‐Parietal Lobe Infarction Appearing After Reperfusion by Recombinant Tissue Plasminogen Activator

Abstract

Hemichorea-hemiballism (HC-HB) is classically associated with stroke lesions in the STN.1-3 A large clinical study reported that some other lesions in the basal ganglia, such as in the caudate and putamen, may also cause HC-HB, 4 which is seldom the result of a cortical infarction. We observed transient HC-HB in a patient with a cerebral infarction in the temporal-parietal lobe without any lesions in the basal ganglia including the STN after intravenous recombinant tissue plasminogen activator (rtPA) administration.A 72-year-old right-handed female, who had neither a history of diabetes mellitus nor dopaminergic medication use, was admitted to our hospital because of sudden-onset leftsided hemiparesis. Neurological examination revealed spatial disorientation, conjugate eye deviation to the right, and dysarthria. She had left-sided hemiparesis and sensory disturbance of all modalities. Deep tendon reflexes were exaggerated in the affected limbs. The plantar response was bilaterally flexor. National Institutes of Health Stroke Scale (NIHSS) was 19 points on admission. Blood sample tests were normal except for elevations of brain natriuretic peptide (717 pg/mL) and D-dimer (10.3 lg/mL). Thyroid function was normal, and hyperglycemia was ruled out. Brain MRIs showed acute cerebral infarction in the right temporal-parietal lobe perfused by the middle cerebral artery (MCA; Fig. 1A,B). Electrocardiogram showed atrial fibrillation. The patient was diagnosed as having cardioembolic infarction, and rtPA was administered within 3 hours after onset of symptoms. Nine hours later, her hemiparesis was improved significantly, which was reflected in the NIHSS score of 8 points (11-point decrease). Subsequent to motor improvement, the left hand started to show choreic movements, such as stereotypic pronation and supination, which progressed into ballistic arm movements in a day's time. Eventually, the left-lower extremity was also involved, confirming HC-HB syndrome (Video 1). Subsequent brain MRIs confirmed no lesions in the basal ganglia, including the STN, and no changes in size of the stroke lesion (Fig. 1C,D). Single-photon emission CT (SPECT) showed an increase of blood flow in the right basal ganglia and hypoperfusion in the affected cortical lesion (Fig. 1E). These involuntary movements persisted and disappeared on the ninth day. She no longer exhibited neurological deficits thereafter. Five months later, follow-up brain MRIs revealed cortical laminar necrosis with atrophic changes in the stroke lesion, but no lesions in the basal ganglia (Fig. 1F).Hyperkinetic involuntary movements accompanied by a pure cortical infarction sparing the basal ganglia are extremely rare. The aforementioned large clinical study reported that only 6 cases of 5,007 consecutive stroke patients had hemichorea (0.12%), and the lesions were located in the MCA territory. 4 In patients with an STN lesion, hyperkinetic disorder can be explained by dysfunction of the basal ganglia in the motor loop: Reduction of the striatopallidal inhibitory network b...

Delayed Hemichorea Following Temporal–Occipital Lobe Infarction

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Transient Hemiballismus Induced by High G in a Fast Jet Pilot

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“…Murakami et al previously described a 72‐year‐old lady who developed left‐hand chorea within hours of thrombolysis therapy for acute ischaemic stroke, shortly followed by self‐resolving hemiballismus . Whereas MRI showed no basal ganglia abnormalities, nuclear medicine imaging (single‐photon emission computed tomography) revealed increased blood flow to the right basal ganglia, making reperfusion injury the most likely cause for the attack …”

Delayed Hemichorea Following Temporal-Occipital Lobe Infarction

“…A case of temporal–parietal lobe infarct showed reduced perfusion in the ipsilateral basal ganglion, and a series of three patients with cortical strokes showed no perfusion changes in the basal ganglia or thalamus. 7 , 8 It is possible that some cases of hemichorea result from an interruption of cortical projections to the basal ganglia, but others arise following an interruption of inter-cortical network leading to sensorimotor disintegration. 8 Current management of hemichorea involves the use of antidopaminergic agents or benzodiazepines.…”